H3K27me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA776264 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16635988_1.fastq.gz | Fastqsanger.gz | |||
| SRR16635988_2.fastq.gz | Fastqsanger.gz | |||
| SRR16635989_1.fastq.gz | Fastqsanger.gz | |||
| SRR16635989_2.fastq.gz | Fastqsanger.gz | |||
| SRR16635990_1.fastq.gz | Fastqsanger.gz |
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Project description:H3K4me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His
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Project description:Stem cells reside in specialized niches that play a critical role in modulating their fate. Supporting cells in the niche instruct fate changes to the stem cells through epigenetic enzymes that transduce cell signaling to modify gene expression. Recent studies showed that the innate immune response to muscle injury alters the muscle stem cell (MuSC) niche, it remains unknown how MuSC adapt to the modified milieu to mediate muscle repair. Here we show that the epigenetic enzyme JMJD3 coordinates MuSC adaptation to the regenerative niche in a non-cell autonomous manner where it modifies their extracellular matrix to integrate signaling that stimulates exit of quiescence. Genomics and transcriptomics approaches identified the hyaluronic acid (HA) synthesis enzyme Has2 as a key JMJD3 target gene that allows MuSCs to integrate signals from the regenerative niche. Overall, we identified a specific role for JMJD3 in regulating the expression of genes that allow MuSCs to adapt to the modified niche of regenerating muscle. We aim to determine the differential occupancy of histone H3 lysine 4 trimethyl mark muscle satellite stem cells isolated from JMJD3scKO, UTXscKO and Wild-type mice.
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Project description:Stem cells reside in specialized niches that play a critical role in modulating their fate. Supporting cells in the niche instruct fate changes to the stem cells through epigenetic enzymes that transduce cell signaling to modify gene expression. Recent studies showed that the innate immune response to muscle injury alters the muscle stem cell (MuSC) niche, it remains unknown how MuSC adapt to the modified milieu to mediate muscle repair. Here we show that the epigenetic enzyme JMJD3 coordinates MuSC adaptation to the regenerative niche in a non-cell autonomous manner where it modifies their extracellular matrix to integrate signaling that stimulates exit of quiescence. Genomics and transcriptomics approaches identified the hyaluronic acid (HA) synthesis enzyme Has2 as a key JMJD3 target gene that allows MuSCs to integrate signals from the regenerative niche. Overall, we identified a specific role for JMJD3 in regulating the expression of genes that allow MuSCs to adapt to the modified niche of regenerating muscle. We aim to determine the differential occupancy of histone H3 lysine 4 trimethyl mark muscle satellite stem cells isolated from JMJD3scKO, UTXscKO and Wild-type mice.
2022-08-04 | GSE186829 | GEO
Project description:Stem cells reside in specialized niches that play a critical role in modulating their fate. Supporting cells in the niche instruct fate changes to the stem cells through epigenetic enzymes that transduce cell signaling to modify gene expression. Recent studies showed that the innate immune response to muscle injury alters the muscle stem cell (MuSC) niche, it remains unknown how MuSC adapt to the modified milieu to mediate muscle repair. Here we show that the epigenetic enzyme JMJD3 coordinates MuSC adaptation to the regenerative niche in a non-cell autonomous manner where it modifies their extracellular matrix to integrate signaling that stimulates exit of quiescence. Genomics and transcriptomics approaches identified the hyaluronic acid (HA) synthesis enzyme Has2 as a key JMJD3 target gene that allows MuSCs to integrate signals from the regenerative niche. Overall, we identified a specific role for JMJD3 in regulating the expression of genes that allow MuSCs to adapt to the modified niche of regenerating muscle. We aim to determine the differential occupancy of histone H3 lysine 4 trimethyl mark muscle satellite stem cells isolated from JMJD3scKO, UTXscKO and Wild-type mice.
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Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we assayed for genome-wide localization of JMJD3 enrichment. This piece of data was further integrated to expression changes using RNA sequencing as well as ChIP-Sequencing analysis of H3K27me3 upon genomic/genetic knock-down or chemical inhibition of JMJD3 and UTX. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to identify a hitherto unknown role of JMJD3 as an oncogenice facilitator in leukemia whereas UTX plays a tumor suppressor role. JMJD3 ChIP: 10 million cells were used for the ChIP and precipitated using 10micrograms of antibody (abgent, AP1022a) against human JMJD3.
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Project description:The level of H3K27me3 were examined by conditional knockout Ezh2, Utx or Jmjd3 in mouse chondrocyte
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Project description:The object of this study was to explore whether the loss of mRNA decapping in the Arabidopsis mutant tdt-1 resulted in global dfferences of RNA profiles, as compared to wild type. Experiment Overall Design: In this experiment we compared expression in tdt-1 and wild type 3 day whole seedlings. We performed three biological replicates, in which one experiment was dye-swapped.
2008-06-15 | E-GEOD-7359 | biostudies-arrayexpress
Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we chemically inhibited the H3K27me3 demethylase JMJD3 using the GSKJ4 inhibitor and assayed for genome-wide changes in H3K27me3 and JMJD3 enrichment. This piece of data was further integrated to expression changes using RNA sequencing as well as ChIP-Sequencing analysis of H3K27me3 upon genomic knock-down of JMJD3 and UTX. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to identify a hitherto unknown role of JMJD3 as an oncogenice facilitator in leukemia whereas UTX seems to play a tumor suppressor role. Histone ChIP: Half to one million cells were treated with micrococcal nuclease (MNASE) to generate mononucleosomal particles and an adaptation of the Upstate ChIP protocol was used.
2014-10-01 | E-GEOD-56693 | biostudies-arrayexpress
Project description:Autophagy is essential for cellular survival and energy homeostasis under nutrient deprivation. Despite the emerging importance of nuclear events in autophagy regulation, epigenetic control of autophagy gene transcription remains unclear. Here, we identify Jumonji-D3 (JMJD3/KDM6B) histone demethylase as a key epigenetic activator of hepatic autophagy. Upon fasting-induced fibroblast growth factor-21 (FGF21) signaling, JMJD3 epigenetically upregulated global autophagy-network genes, including Tfeb, Atg7, Atgl, and Fgf21, through demethylation of histone H3K27-me3, resulting in autophagy-mediated lipid degradation. Mechanistically, phosphorylation of JMJD3 at Thr-1044 by FGF21 signal-activated PKA increased its nuclear localization and interaction with the nuclear receptor PPARto transcriptionally activate autophagy. Chronic administration of FGF21 in obese mice improved defective autophagy and hepatosteatosis in a JMJD3-dependent manner. Remarkably, in non-alcoholic fatty liver disease patients, hepatic expression of JMJD3, ATG7, LC3, and KL were substantially decreased. These findings demonstrate that FGF21-JMJD3 signaling epigenetically links nutrient deprivation with hepatic autophagy and lipid degradation in mammals
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